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The effects of two specific inhibitors of protein kinase C (PKC) on fever and release of interleukin-6 (IL-6) in rats injected with endotoxin lipopolysaccharide (LPS) were studied. Results showed that in vivo injection of the inhibitors reduced LPS-induced fever and attenuated elevation of plasma IL-6. Data indicated differences consistent with their potency as inhibitors of PKC. Combined administration of an inhibitor and the glucocorticoid dexamethasone enhanced the antipyretic effect without affecting the induced elevation of IL-6.

An experiment was conducted to determine the effects of heat exposure on the development of fever in rats induced by endotoxin lipopolysaccharide (LPS). Results showed significantly higher fevers for rats injected with LPS 24 hrs after heat exposure. Heat-stressed rats also exhibited decrease in body weight and reduced plasma tumor necrosis factor (TNF) concentration. Findings also indicated evidence of inducible HSP-70 accumulated for heat stressed rats. It is suggested that attenuated changes in serum iron and higher fevers are caused by the reduction in TNF.

The effects of dietary n-3 fatty acids on several aspects of sickness behavior due to inflammation were analyzed in mice after subcutaneous injections of turpentine and lipopolysaccharides (LPL). Analysis of sickness behavior in turpentine- and LPL-treated mice indicated the role of fish oil diets in reducing LPL- and turpentine-induced fever, lethargy, anorexia and weight decrease. Dietary fish oil supplementation-induced resistance to LPL-inflammation also involved the suppression of prostaglandin E2 by n-3 fatty acids.

The role of interleukin-6 (IL-6) in the regulation of symptoms of sickness behavior caused by turpentine and influenza pneumonitis was analyzed in IL-6 knockout mice. Subcutaneous injections of turpentine in IL-6-knockout mice did not induced the development of fever, anorexia and cachexia due to the absence of IL-6. The IL-6-knockout mice also exhibited slightly modified symptoms of sickness behavior during influenza virus infection. The sickness behavior of IL-6-knockout mice indicated the critical role of IL-6 in inducing inflammation due to turpentine.

Mice with interleukin-1 type I receptors (IL-1Rt1) and knockout mice were injected with turpentine to determine the effects of endogenous interleukin-1 receptors on inflammation response. The knockout mice and mice with IL-1Rt1 exhibited fever, suppressed motor activity or anorexia after the administration of turpentine. Furthermore, turpentine-induced anorexia was similar in knockout mice without IL-1Rt1 and mice with IL-1Rt1.

Mammalian bodies become unable to regulate body temperature when attacked by viruses and pathological microbes if they are deficient in interleukin-beta (Il-B). Infections introduce lipopolysaccharides and other cell debris which are supposed to induce a fevered condition, but Il-B deficient mice have lower fevers 24 hours after a viral attack. They were also more likely to die when exposed to the influenza virus.

Antiserums to tumor necrosis factor (TNF) and soluble tumor necrosis factor receptor (sTNFR) block a decrease in core temperature that normally precedes fever in mice following injections of lipopolysaccharide (LPS) and enhances the duration of increased temperatures independent of the maximum febrile temperature. Thus, TNF-alpha likely affects the endogenous system that reduces core temperature.

A study of the acute phase of mice after intranasal inoculation with the mouse-adapted influenza viral doses with varying lethalities reveals elevated levels of cytokines in the lungs, indicating that physiological and behavioral variations during acute influenza infections are mediated by cytokines. Low-dose inoculation lowers water and food intake significantly, accompanied by general locomotor activity and body temperature decreases six days after inoculation, while high-dose inoculation induces these changes within 48 hours after inoculation.

Characterization of the fundamental biology of fever to lipopolysaccharide (LPS) in unrestrained mice confirm the possibility of major and reproducible fevers in response to LPS which is unique in terms of time course, dose-dependent profile, induction of pyrogenic tolerance profile and mode of inhibition by indomethacin. Suppression of locomotor activity accompanies variations in body temperature.

A study was conducted to examine the peripheral and intrahypothalamic discharges of interleukin-6 (IL-6) and tumor necrosis factor (TNF) during fever caused by bacterial lipopolysaccharide in guinea pigs. The relation of various stages of fever to different central or peripheral functions of IL-6 and TNF was also examined. The results revealed that a physiological condition in which generation and discharge of cytokines in the peripheral immune system and in the hypothalamus are controlled and incited in separate patterns by endotoxin fever.

A decline in motor activity, weight decrease and anorexia were caused by the development of tumors. The methylcholanthrene sarcoma was used to ascertain the link between interleukin-6, systemic levels of tumor necrosis factor and the temporal patterns arising from the cachectic impact of tumor development. There was a drop in body temperature and water intake was augmented three-fold.

Experiments were conducted to determine if the modulation of the febrile and cytokine responses of rats by glucocorticoids is caused by the elevation of this stress hormone or by its permissive effects. This involved the administration of varying doses of replacement corticosterone to adrenaloctomized (ADX) rats. The febrile response of ADX rats were compared to those of sham-ADX rats provided with placebo pellets. Results indicate that changes in intact rats due to glucocorticoids are not permissive.

Abstract Background Obesity is a common pathology with increasing incidence, and is associated with increased mortality and healthcare costs. Several treatment options for obesity are currently available ranging from behavioral modifications to pharmaceutical agents. Many popular dietary supplements claim to enhance weight loss by acting as metabolic stimulators, however direct tests of their effect on metabolism have not been performed. Purpose This work identified the effects popular dietary supplements on metabolic rate and mitochondrial biosynthesis in human skeletal muscle cells. Methods Human rhabdomyosarcoma cells were treated with popular dietary supplements at varied doses for 24 hours. Peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1α), an important stimulator of mitochondrial biosynthesis, was quantified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Mitochondrial content was measured using flow cytometry confirmed with confocal microscopy. Glycolytic metabolism was quantified by measuring extracellular acidification rate (ECAR) and oxidative metabolism was quantified by measuring oxygen consumption rate (OCR). Total relative metabolism was quantified using WST-1 end point assay. Results Treatment of human rhabdomyosarcoma cells with dietary supplements OxyElite Pro (OEP) or Cellucore HD (CHD) induced PGC-1α leading to significantly increased mitochondrial content. Glycolytic and oxidative capacities were also significantly increased following treatment with OEP or CHD. Conclusion This is the first work to identify metabolic adaptations in muscle cells following treatment with popular dietary supplements including enhanced mitochondrial biosynthesis, and glycolytic, oxidative and total metabolism.

Abstract Background Polyunsaturated fatty acids are popular dietary supplements advertised to contribute to weight loss by increasing fat metabolism in liver, but the effects on overall muscle metabolism are less established. We evaluated the effects of conjugated linoleic acid (CLA) or combination omega 3 on metabolic characteristics in muscle cells. Methods Human rhabdomyosarcoma cells were treated with either DMSO control, or CLA or combination omega 3 for 24 or 48 hours. RNA was determined using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Mitochondrial content was determined using flow cytometry and immunohistochemistry. Metabolism was quantified by measuring extracellular acidification and oxygen consumption rates. Results Omega 3 significantly induced metabolic genes as well as oxidative metabolism (oxygen consumption), glycolytic capacity (extracellular acidification), and metabolic rate compared with control. Both treatments significantly increased mitochondrial content. Conclusion Omega 3 fatty acids appear to enhance glycolytic, oxidative, and total metabolism. Moreover, both omega 3 and CLA treatment significantly increase mitochondrial content compared with control.

Physical activity (PA) in children/adolescents of both genders from a rural community in Mozambique was estimated by accelerometry and by questionnaire and was compared with PA of Portuguese youth. Total PA, moderate (MPA), vigorous (VPA) and very vigorous (VVPA) were evaluated. Mozambican boys were more active than girls. Intensity of PA declined significantly with age. Survival activities, such as household tasks, were the predominant mode of PA. Compared with Portuguese children/adolescents, Mozambicans had significantly higher total PA; showed less decline of PA with age and engaged in fewer minutes at higher intensity PA. Environmental factors likely explain documented differences. [ABSTRACT FROM AUTHOR]